EYE FATIGUE RELIEF
are you tired or being tired?
The advances of information technology, software and electronics have led to the widespread use of screen based equipment or Visual Display Terminals (VDT) for both work and leisure. According to The National Center for Education Statistics, about 90 percent of children and adolescents in developed countries, ages 5 to 17, use computers at school or at home. About 50 percent of 9-year-olds use the Internet and at least 75 percent by ages 15 to 17.
This phenomenon often lead to asthenopia or eye fatigue. The symptoms include sensitivity to glare, headaches, sore eyes and blurred vision. A recent study conducted by the National Institute of Occupational Safety and Health in USA found that over 90 percent of habitual users of VDT reported eyestrain and other visual problems associated with computer use. The American Optometric Association supported this in a survey reporting that between 50 and 75 percent of all VDT workers report eye problems. In another study conducted in Sweden, 23 percent of schoolchildren, aged 6-15 suffered from asthenopia-related symptoms (Anshel, 2009).
Asthenopia prompted a large number of occupational safety studies. For example, epidemiological studies over the last decade revealed significant factors that contribute to eye fatigue. These studies, sometimes involving up to 6,000 sufferers identified the following causes: insufficient lighting, poor ergonomics and uncorrected vision. Despite the new information, follow-up studies later showed that the implemented improvements were only effective in 50% of sufferers. The possible explanations for this observation could be that other factors remained undiscovered, poor implementation of improvements, or visual work had become even more visually demanding. It is likely to be a combination of these factors so that current solutions are insufficient to reduce asthenopia.
Standardized questionnaires that assessed subjective eye fatigue symptoms are in most cases mild, but symptoms get progressively worse if the causes are not rectified. Furthermore, certain ophthalmological tests can also detect eye problems, for example accommodation amplitudes, rate of accommodative reaction (positive and negative directions), critical flicker fusion (CFF) and pattern visual evoked potential (PVEP). So far, 10 Japanese clinical studies conducted by 9 independent ophthalmological establishments were able to conclude the efficacy of astaxanthin to alleviate visual asthenopia by observed improvements in the accommodation function and recovery of the ciliary body (Figure 1); retinal blood flow and inflammation markers.
Figure 1. Location of the ciliary body in the human eye
ASTAXANTHIN REDUCES EYE FATIGUE
Asthenopia (eye fatigue) occurs on a daily cycle, in that the visual performance generally decreases naturally from morning until night. This problem exacerbates with a daily VDT load that lasts between 4 to 7 hours by affecting the accommodation performance of the ciliary body, which controls lens refraction. A couple of randomized double blind placebo controlled pilot studies demonstrated the positive effects of astaxanthin supplementation on visual function. For example, a study by Nagaki et al., (2002), demonstrated that subjects (n=13) who received 5 mg astaxanthin per day for one month showed a 54% reduction of eye fatigue complaints (Figure 2). In a sports vision study led by Sawaki et al., (2002), they demonstrated that depth perception and critical flicker fusion had improved by 46% and 5% respectively on a daily dose of 6 mg (n=9). The effect of astaxanthin on visual performance prompted a number of other clinical studies to evaluate the optimum dose and identify the mechanism of action.
Figure 2. VDT Subjects with Eye Strain Symptoms before and after astaxanthin supplementation (Nagaki et al.,2002)
Overall eye fatigue symptoms improve with astaxanthin based on a questionnaire at 4 weeks
A study by Nakamura (2004), demonstrated significant improvements in reducing asthenopia and positive accommodation for the 4 mg (p<0.05) and 12 mg (p<0.01) groups. However, it was not until Nitta et al., (2005), who established the optimum daily dose at 6 mg (n=10) for a period of 4 weeks by comparing eye fatigue using a visual analogue scale (VAS) based questionnaire and accommodation values. Overall, the 6 mg group improved significantly better at week 2 and 4 of the test period. Furthermore, questionnaire results obtained by Shiratori et al., (2005) and Nagaki et al., (2006), also confirmed the previous findings that astaxanthin supplementation at 6 mg for 4 weeks improved symptoms associated with tiredness, soreness, dryness and blurry vision. Another study by Takahashi & Kajita (2005), also demonstrated that astaxanthin attenuates induced-eye fatigue, as opposed to treating eye fatigue, which suggests prevention rather than treatment. Astaxanthin treated groups (asthenopia negative) were able to recover quicker than the control group after heavy visual stimulus. Later, Iwasaki & Tawara (2006) also confirmed the same tendencies of subjective eye fatigue complaints in a randomized double-blind placebo controlled double-crossover study.
In addition to questionnaires, direct measurement associated with asthenopia is also strong indicators for understanding astaxanthin efficacy. These include accommodation amplitude (Figure 3); rate of accommodation reaction (positive and negative directions); CFF (critical flicker fusion) and PVEP (pattern visual evoked potential).
Based on the quantitative information, the accommodation related measurements consistently improved after the treatment period (Nagaki et al., 2002, 2006; Nakamura et al., 2004; Takahashi & Kajita, 2005; Shiratori et al., 2005; Nitta et al., 2005; Iwasaki & Tawara, 2006) whereas the CFF and PVEP remained inconclusive (Sawaki et al., 2002; Nagaki et al., 2002; Nakamura et al., 2004). Therefore, the mechanism by which astaxanthin improved eye fatigue strongly indicates accommodation.
Figure 3. Objective accommodation (Nitta et al., 2005)
Objective accommodation amplitude improves with 6mg astaxanthin.
MECHANISM OF ACTION
Accommodation measures the lens refractive property and it corresponds to the ciliary body function. This small ocular muscle controls the lens thickness in order to focus the light on the retina. In heavy visual workloads, the eye is focused on a fixed object distance for extended periods that will cause muscle spasms or develop fatigue detectable by accommodation tests. These tests are interrelated and include the following: accommodation amplitude; accommodation reaction (positive or negative) and high frequency component (HFC). Each clinical study used a combination of accommodation tests to indicate the amount of fatigue present. For example, increased accommodation amplitude in all treated subjects indicated improved reaction on near and far objects (Nagaki et al., 2002, 2006; Nakamura et al., 2004). Figure 4, Figure 5 and Table 1 reveal the higher rate of accommodation reactions measured in astaxanthin treated groups. These indicate the speed at which the ciliary body reacted to the direction change of focus (negative accommodation means from a near object at 35 centimeters to distant object at 5 meters or vice versa); (Nitta et al., 2005; Shiratori et al., 2005; Nakamura et al., 2005; Iwasaki & Tawara, 2006). The effects of astaxanthin are significant from 2 weeks.
Table 1. Improvement of negative accommodation time with astaxanthin (Iwasaki & Tawara, 2006)
2.Increase Blood Flow
Another randomized placebo controlled study by Nagaki et al., (2005) detected the increase of retinal blood flow in the astaxanthin treated group that received 6 mg for 4 weeks (n=14, p<0.01). Even though the precise reason for accommodation improvement seen with astaxanthin is not yet clear, the author postulated that based on the rheological improvement measured in the retinal capillary vessels, most likely means more blood also reaches the ciliary body and provides more nourishment to the ciliary muscles. Furthermore, the rheological improvement agreed with Nagaki et al., (2005) who studied ten healthy subjects treated with 6 mg astaxanthin for ten days (Figure 7). The blood exhibited significantly higher flow rates (ex-vivo) compared to the control group (p<0.05) utilizing the micro-array channel flow analyzer (MC-FAN).
Figure 7. Increase of retinal blood flow (Nagaki et al., 2005)
Retinal blood flow increases with astaxanthin after 4 weeks.
Lastly, a top Japanese ophthalmology research collaboration between Hokkaido, Yokohama and Tokyo concluded anti-inflammatory properties of astaxanthin in endotoxin-induced uveitis (EIU or eye inflammation) both in vivo and in vitro models. Ohgami et al., (2003) observed in a dose dependant fashion that astaxanthin doses of 1, 10 or 100mg/kg dose in rats had the same anti-inflammatory action as 10 mg/kg prednisolone (n=8, p<0.01). Inflammation markers such as nitric oxide synthase (NOS), prostaglandin E2 (PGE2) and tumor necrosis factor (TNF)- α were all significantly reduced. In human terms, 4 mg astaxanthin per day may deliver the same benefits as 4 mg prednisolone without the side effects of intraocular pressure build-up. Other reduced biomarkers were cellular infiltration and protein build up in the aqueous humor - watery substance filling the space between the lens and the cornea.
Another study conducted by Hashimoto et al., (2009) found that oral administration of 6mg of astaxanthin for 2 weeks increased free radicals scavenging activity in the aqueous humor by 10 percent (p<0.01) in non-diabetic male patients (n=7) and 15 percent (p<0.01) in diabetic male patients (n=9). The aqueous humor serves a very important function since it provides nutrients to the lens and corneal endothelium, maintains the convex shape of the cornea and carries away waste products from ocular tissues.
In another study, Suzuki et al., (2006) confirmed the same effects while they carefully studied the anti-inflammatory effect of astaxanthin in the iris-ciliary body of rat eyes. This was also the first study to prove that astaxanthin suppressed NF-kB activation by free radicals in the EIU rat model (Figure 8). The result is a lower pro-inflammatory response that would otherwise perpetuate local sites of inflammation that may also help explain why astaxanthin worked to alleviate eye fatigue in numerous clinical trials.
Figure 8. Number of NF-κB positive cells in eye ciliary body during inflammation (Suzuki et al., 2006)
Astaxanthin reduced the number of inflamed cells in the ciliary body.
Eye fatigue or asthenopia is a common problem that occurs with the regular use of VDTs and may be resolved with findings from many worldwide epidemiological studies. However, if current improvements tend to be only 50% successful and other factors are likely to be involved, therefore, based on the current clinical evidence, astaxanthin offers a complementary alternative by reducing inflammation, improving accommodation and increasing blood flow